ArticleThe Journal of physiology2003
Amplification of exocytosis by Ca2+-induced Ca2+ release in INS-1 pancreatic beta cells.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Therapeutic Potential of GLP-1 Receptor Agonists in Diabetes and Cardiovascular Disease: Mechanisms and Clinical Implications.Cardiovascular drugs and therapy · 2026Review
- Imeglimin amplifies glucose-stimulated insulin release from diabetic islets via a distinct mechanism of action.PloS one · 2021Article
- ATP-sensitive KPflugers Archiv : European journal of physiology · 2019Article
- Sodium current inhibition following stimulation of exchange protein directly activated by cyclic-3',5'-adenosine monophosphate (Epac) in murine skeletal muscle.Scientific reports · 2019Article
- Pleiotropic Effects of GLP-1 and Analogs on Cell Signaling, Metabolism, and Function.Frontiers in endocrinology · 2018Review
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Arrhythmic effects of Epac-mediated ryanodine receptor activation in Langendorff-perfused murine hearts are associated with reduced conduction velocity.Clinical and experimental pharmacology & physiology · 2017Article
- Quercetin potentiates transdifferentiation of bone marrow mesenchymal stem cells into the beta cells in vitro.Journal of endocrinological investigation · 2017Article
- Modeling analysis of inositol 1,4,5-trisphosphate receptor-mediated Ca2+ mobilization under the control of glucagon-like peptide-1 in mouse pancreatic β-cells.American journal of physiology. Cell physiology · 2016Article
- Ca2+ influx through L-type Ca2+ channels and Ca2+-induced Ca2+ release regulate cAMP accumulation and Epac1-dependent ERK 1/2 activation in INS-1 cells.Molecular and cellular endocrinology · 2016Article
- Caffeine, Through Adenosine A3 Receptor-Mediated Actions, Suppresses Amyloid-β Protein Precursor Internalization and Amyloid-β Generation.Journal of Alzheimer's disease : JAD · 2015Article
- New insights concerning the molecular basis for defective glucoregulation in soluble adenylyl cyclase knockout mice.Biochimica et biophysica acta · 2014Review
- Regulation of glucose homeostasis by GLP-1.Progress in molecular biology and translational science · 2014Review
- Quercetin induces insulin secretion by direct activation of L-type calcium channels in pancreatic beta cells.British journal of pharmacology · 2013Article
- GLP-1 receptor activated insulin secretion from pancreatic β-cells: mechanism and glucose dependence.Diabetes, obesity & metabolism · 2013Review
- Role of phospholipase Cε in physiological phosphoinositide signaling networks.Cellular signalling · 2012Review
- Molecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic β cells.Progress in biophysics and molecular biology · 2011Review
- Ca-induced Ca Release from Internal Stores in INS-1 Rat Insulinoma Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Epac2-dependent mobilization of intracellular Ca²+ by glucagon-like peptide-1 receptor agonist exendin-4 is disrupted in β-cells of phospholipase C-ε knockout mice.The Journal of physiology · 2010Article
- PKA-dependent potentiation of glucose-stimulated insulin secretion by Epac activator 8-pCPT-2'-O-Me-cAMP-AM in human islets of Langerhans.American journal of physiology. Endocrinology and metabolism · 2010Article
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Authors and funding
2 authors.
Funding
Abstract
Functional coupling between Ca(2+)-induced Ca(2+) release (CICR) and quantal exocytosis in 5-hydroxytryptamine-loaded INS-1 beta cells was assessed through the use of carbon fibre amperometry in combination with Fura-2. CICR was evoked by the glucagon-like-peptide-1 (GLP-1) receptor agonist exendin-4 (Ex-4) and was accompanied by quantal secretory events appearing as amperometric current spikes time-locked to the increase of [Ca(2+)](i). The action of Ex-4 was reproduced by treatment with caffeine, and the source of Ca(2+) serving as a stimulus for exocytosis originated from ryanodine and thapsigargin-sensitive Ca(2+) stores. Two distinct patterns of exocytosis occurred within 5 s following the initiation of CICR. Non-summating exocytosis (NS-type) was defined as multiple asynchronous current spikes, and the half-height duration of each spike was 12-48 ms. Summating exocytosis (S-type) was defined as a cluster of spikes. It generated a macroscopic current, the half-height duration of which was 243-682 ms. The release charge of S-type exocytosis was 3.2-fold greater than that of NS-type when measured 2 s following the initiation of secretion. NS-type exocytosis was observed frequently under conditions in which the basal Ca(2+) concentration ([Ca(2+)](B)) was low (75-150 nM), whereas S-type exocytosis predominated under conditions in which the [Ca(2+)](B) was elevated (200-275 nM). Depolarization-induced Ca(2+) influx triggered NS-type exocytosis in most cells tested, irrespective of [Ca(2+)](B). It is concluded that CICR is a highly effective stimulus for exocytosis in INS-1 cells. The increase of [Ca(2+)](i) that accompanies CICR stimulates the asynchronous release of a small number of secretory granules under conditions of low [Ca(2+)](B). When [Ca(2+)](B) is slightly elevated, CICR targets a much larger pool of secretory granules that undergo summating exocytosis. The transition from NS-type to S-type exocytosis may represent an amplification mechanism for Ca(2+)-dependent exocytosis.
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